In this review, we summarize and analyze the possible mechanisms underlying the resistance to ICIs in NSCLC with KRAS mutation and mainly focus on the role of the tumor microenvironment (TME) and metabolism, therapeutic implications, and potential targets for overcoming the resistance to or improving the efficacy of ICIs treatments in KRAS-mutant NSCLC. This evidence concerns the gene KRAS and non-small cell lung carcinoma.